Search

Oral neomycin administration impacts the gut microbiome and delays vitiligo development in mice, and topical antibiotics may likewise allow the microbiome to preserve skin health and delay depigmentation. Here, we examined the effects of 6‐week topical antibiotic treatment on vitiligo‐prone pmel‐1 mice. Bacitracin, Neosporin, or Vaseline were applied to one denuded flank, while the contralateral flank was treated with Vaseline in all mice. Ventral depigmentation was quantified weekly. We found that topical Neosporin treatment significantly reduced depigmentation and exhibited effects beyond the treated area, while Bacitracin ointment had no effect. Stool samples collected from four representative mice/group during treatment revealed that Neosporin treatment aligned with reduced abundance of the Alistipes genus in the gut, while relevant changes to the skin microbiome at end point were less apparent. Either antibiotic treatment led to reduced expression of MR1, potentially limiting mucosal‐associated invariant T‐cell activation, while Neosporin‐treated skin selectively revealed significantly reduced CD8+ T‐cell abundance. The latter finding aligned with reduced expression of multiple inflammatory markers and markedly increased regulatory T‐cell density. Our studies on favorable skin and oral antibiotic treatment share the neomycin compound, and in either case, microbial changes were most apparent in stool samples. Taken together, neomycin‐containing antibiotic applications can mediate skin Treg infiltration to limit vitiligo development. Our study highlights the therapeutic potential of short‐term antibiotic applications to limit depigmentation vitiligo. [ABSTRACT FROM AUTHOR]

Background and Aims: Diabetic foot ulcers (DFUs) add billions of dollars to the direct annual costs associated with diabetes. Despite various treatments, many DFUs do not heal and become infected. Both skin‐associated microbial communities and glycemic control are believed to be important in nonhealing DFUs. Recent studies have linked serum Vitamin C levels with glycemic control and DFUs. This cross‐sectional study assessed skin microbiome in DFUs, intact diabetic skin, and nondiabetic skin to identify correlations between hemoglobin A1c (HbA1c), Vitamin C, and microbial community structure. Correlations between Vitamin C, HbA1c, wound size, and ulcer duration were also determined. Methods: Participants had their DFUs or intact skin culture swabbed. HbA1c was obtained via point‐of‐care fingerstick testing and serum Vitamin C was obtained via venipuncture. All participants completed a dietary questionnaire. Participants with ulcers were stratified into the controlled (≤8.0%) or uncontrolled (>8.0%) HbA1c group. Analysis of microbial communities was performed via 16S ribosomal RNA (rRNA) gene amplicon sequencing and bacterial load was measured by the domain‐level quantitative polymerase chain reaction of the 16S rRNA gene. Results: Forty‐two patients were recruited over 6 months. Bacteria from the genera Staphylococcus and Stenotrophomonas were present in all samples and often dominant, but a shift towards anaerobic pathogenic taxa was observed in ulcers. No global significant differences were observed for HbA1c and Vitamin C levels in the microbial community structure (R < 0.013/p > 0.375). Bacterial loads were 4–5 orders of magnitude higher in ulcers than in intact skin samples. Bacterial load was not significantly higher in the uncontrolled HbA1c group (p = 0.67). Larger wound sizes (p = 0.46) were observed in the uncontrolled HbA1c group compared to the control. Lower Vitamin C levels (p = 0.002) were observed in the uncontrolled HbA1c group compared to nondiabetic controls. Conclusion: Understanding the link between Vitamin C and HbA1c and DFU microbiome may aid in new therapies. [ABSTRACT FROM AUTHOR]

Background: The degradation in soil quality over the last four decades poses a major threat to the sustainability of the puddled transplanted rice (Oryza sativa L.) system in southern China. Conservation tillage practices (CTPs) such as no‐tillage and crop straw mulching (SM) are considered effective strategies for achieving sustainable crop production. Aims: This study aimed to assess the efficacy of different CTPs on crop yield and soil properties in an ongoing long‐term field experiment (2008–2020), particularly changes in soil chemical properties and enzymatic activities and their relationship with rice grain yield. Methods: Five treatments including conventional tillage (CT), CT and straw retention, CT and SM (CT‐SM), no‐tillage (NT), and NT and SM (NT‐SM) were applied at a field scale over a period of 12 years. In Years 11 (2019) and 12 (2020), soil samples were collected at two depths (0–10 cm and 10–20 cm) after rice harvesting. Soil chemical traits, enzymatic activities, and rice production were measured in response to different CTPs treatments, and differences between treatments were assessed. Results: Soil pH, soil organic carbon, total nitrogen (N), available N, total phosphorus (P), and available P were significantly higher in CTP treatments, compared with CT. The activities of soil enzymes including invertase, acid phosphatase, urease, catalase, β‐glucosidase, and cellulase were significantly higher in CTP soils, compared with CT soils. A general trend of lower enzyme activity was observed at the deeper soil depth. The NT‐SM treatment fields consistently produced the highest grain yield and larges differences in edaphic properties relative to the CT fields; however, all CTP treatments lead to significant increases in grant yield and edaphic properties relative to CT. A correlation analysis demonstrated that the enhancement in soil enzymatic activities contributed to soil quality and grain yield of rice. Conclusions: The results of this long‐term field study indicate that the use of CTPs in paddy soil can benefit farmers in southern China by improving soil functionality and sustainability and the grain yield of rice. [ABSTRACT FROM AUTHOR]

The article presents a study which discusses association of nasal micro biome and asthma control in patients with chronic rhinosinusitis. Topics include chronic rhinosinusitis (CRS) as a chronic inflammatory disease, completion of an Asthma Control Test (ACT) by asthma patients, and questionnaire that captures information about current asthma control, asthma emergency room(ER) visits and hospitalization.

Background Circadian rhythm disruption is a prevalent feature of modern day society that is associated with an increase in pro-inflammatory diseases, and there is a clear need for a better understanding of the mechanism(s) underlying this phenomenon. We have previously demonstrated that both environmental and genetic circadian rhythm disruption causes intestinal hyperpermeability and exacerbates alcohol-induced intestinal hyperpermeability and liver pathology. The intestinal microbiota can influence intestinal barrier integrity and impact immune system function; thus, in this study, we sought to determine whether genetic alteration of the core circadian clock gene, Clock, altered the intestinal microbiota community. Methods Male Clock Δ19-mutant mice (mice homozygous for a dominant-negative-mutant allele) or littermate wild-type mice were fed 1 of 3 experimental diets: (i) a standard chow diet, (ii) an alcohol-containing diet, or (iii) an alcohol-control diet in which the alcohol calories were replaced with dextrose. Stool microbiota was assessed with 16S ribosomal RNA gene amplicon sequencing. Results The fecal microbial community of Clock-mutant mice had lower taxonomic diversity, relative to wild-type mice, and the Clock Δ19 mutation was associated with intestinal dysbiosis when mice were fed either the alcohol-containing or the control diet. We found that alcohol consumption significantly altered the intestinal microbiota in both wild-type and Clock-mutant mice. Conclusions Our data support a model by which circadian rhythm disruption by the Clock Δ19 mutation perturbs normal intestinal microbial communities, and this trend was exacerbated in the context of a secondary dietary intestinal stressor. [ABSTRACT FROM AUTHOR]

Introduction We showed that Parkinson's disease (PD) patients have alpha-synuclein (α-Syn) aggregation in their colon with evidence of colonic inflammation. If PD patients have altered colonic microbiota, dysbiosis might be the mechanism of neuroinflammation that leads to α-Syn misfolding and PD pathology. Methods Sixty-six sigmoid mucosal biopsies and 65 fecal samples were collected from 38 PD patients and 34 healthy controls. Mucosal-associated and feces microbiota compositions were characterized using high-throughput ribosomal RNA gene amplicon sequencing. Data were correlated with clinical measures of PD, and a predictive assessment of microbial community functional potential was used to identify microbial functions. Results The mucosal and fecal microbial community of PD patients was significantly different than control subjects, with the fecal samples showing more marked differences than the sigmoid mucosa. At the taxonomic level of genus, putative, 'anti-inflammatory' butyrate-producing bacteria from the genera Blautia, Coprococcus, and Roseburia were significantly more abundant in feces of controls than PD patients. Bacteria from the genus Faecalibacterium were significantly more abundant in the mucosa of controls than PD. Putative, 'proinflammatory' Proteobacteria of the genus Ralstonia were significantly more abundant in mucosa of PD than controls. Predictive metagenomics indicated that a large number of genes involved in metabolism were significantly lower in the PD fecal microbiome, whereas genes involved in lipopolysaccharide biosynthesis and type III bacterial secretion systems were significantly higher in PD patients. Conclusion This report provides evidence that proinflammatory dysbiosis is present in PD patients and could trigger inflammation-induced misfolding of α-Syn and development of PD pathology. © 2015 International Parkinson and Movement Disorder Society [ABSTRACT FROM AUTHOR]

Chronic glial activation and neuroinflammation induced by the amyloid-β peptide (Aβ) contribute to Alzheimer's disease ( AD) pathology. APOE4 is the greatest AD-genetic risk factor; increasing risk up to 12-fold compared to APOE3, with APOE4-specific neuroinflammation an important component of this risk. This editorial review discusses the role of APOE in inflammation and AD, via a literature review, presentation of novel data on Aβ-induced neuroinflammation, and discussion of future research directions. The complexity of chronic neuroinflammation, including multiple detrimental and beneficial effects occurring in a temporal and cell-specific manner, has resulted in conflicting functional data for virtually every inflammatory mediator. Defining a neuroinflammatory phenotype ( NIP) is one way to address this issue, focusing on profiling the changes in inflammatory mediator expression during disease progression. Although many studies have shown that APOE4 induces a detrimental NIP in peripheral inflammation and Aβ-independent neuroinflammation, data for APOE-modulated Aβ-induced neuroinflammation are surprisingly limited. We present data supporting the hypothesis that impaired apoE4 function modulates Aβ-induced effects on inflammatory receptor signaling, including amplification of detrimental (toll-like receptor 4-p38α) and suppression of beneficial ( IL-4R-nuclear receptor) pathways. To ultimately develop APOE genotype-specific therapeutics, it is critical that future studies define the dynamic NIP profile and pathways that underlie APOE-modulated chronic neuroinflammation. [ABSTRACT FROM AUTHOR]

Bighead carp ( Hypophthalmichthys nobilis) and silver carp ( H. molitrix) are invasive species and listed as US federally injurious species under the Lacy Act. They have established populations in much of the Mississippi River Basin ( MRB; Mississippi, Illinois, and Missouri rivers) and are capable of producing fertile hybrids and complex introgression. Characterizing the composition of this admixture requires a large set of high-quality, evolutionarily conserved, diagnostic genetic markers to aid in the identification and management of these species in the midst of morphological ambiguity. Restriction site-associated DNA ( RAD) sequencing of 45 barcoded bighead and silver carp from the United States and China produced reads that were aligned to the silver carp transcriptome yielded 261 candidate single nucleotide polymorphisms ( SNPs) with fixed allelic differences between the two species. We selected the highest quality 112 SNP loci for validation using 194 putative pure-species and F1 hybrids from the MRB and putative bighead carp and silver carp pure species from China ( Amur, Pearl and Yangtze rivers). Fifty SNPs were omitted due to design/amplification failure or lack of diagnostic utility. A total of 57 species-diagnostic SNPs conserved between carp species in US and Chinese rivers were identified; 32 were annotated to functional gene loci. Twenty-seven of the 181 (15%) putative pure species were identified as hybrid backcrosses after validation, including three backcrosses from the Amur River, where hybridization has not been documented previously. The 57 SNPs identified through RAD sequencing provide a diagnostic tool to detect population admixture and to identify hybrid and pure-species Asian carps in the United States and China. [ABSTRACT FROM AUTHOR]

A large proportion of reactive nitrogen loss from polar sediments is mediated by denitrification, but microorganisms mediating denitrification in polar environments remain poorly characterized. A combined approach of most-probable-number ( MPN) enumeration, cultivation and physiological characterization was used to describe psychrophilic denitrifying bacterial communities in sediments of three Arctic fjords in Svalbard ( Norway). A MPN assay showed the presence of 103−106 cells of psychrophilic nitrate-respiring bacteria g−1 of sediment. Fifteen strains within the Proteobacteria were isolated using a systematic enrichment approach with organic acids as electron donors and nitrate as an electron acceptor. Isolates belonged to five genera, including Shewanella, Pseudomonas, Psychromonas ( Gammaproteobacteria), Arcobacter ( Epsilonproteobacteria) and Herminiimonas ( Betaproteobacteria) . All isolates were denitrifiers, except Shewanella, which exhibited the capacity for dissimilatory nitrate reduction to ammonium ( DNRA). Growth from 0 to 40° C demonstrated that all genera except Shewanella were psychrophiles with optimal growth below 15° C, and adaptation to low temperature was demonstrated as a shift from primarily C16:0 saturated fatty acids to C16:1 monounsaturated fatty acids at lower temperatures. This study provides the first targeted enrichment and characterization of psychrophilic denitrifying bacteria from polar sediments, and two genera, Arcobacter and Herminiimonas, are isolated for the first time from permanently cold marine sediments. [ABSTRACT FROM AUTHOR]

Summary Technologies for massively parallel sequencing are revolutionizing microbial ecology and are vastly increasing the scale of ribosomal RNA (rRNA) gene studies. Although pyrosequencing has increased the breadth and depth of possible rRNA gene sampling, one drawback is that the number of reads obtained per sample is difficult to control. Pyrosequencing libraries typically vary widely in the number of sequences per sample, even within individual studies, and there is a need to revisit the behaviour of richness estimators and diversity indices with variable gene sequence library sizes. Multiple reports and review papers have demonstrated the bias in non-parametric richness estimators (e.g. Chao1 and ACE) and diversity indices when using clone libraries. However, we found that biased community comparisons are accumulating in the literature. Here we demonstrate the effects of sample size on Chao1, ACE, CatchAll, Shannon, Chao-Shen and Simpson's estimations specifically using pyrosequencing libraries. The need to equalize the number of reads being compared across libraries is reiterated, and investigators are directed towards available tools for making unbiased diversity comparisons. [ABSTRACT FROM AUTHOR]

Methanogenesis was characterized in hypersaline microbial mats from Guerrero Negro, Baja California Sur, Mexico both in situ and after long-term manipulation in a greenhouse environment. Substrate addition experiments indicate methanogenesis to occur primarily through the catabolic demethylation of non-competitive substrates, under field conditions. However, evidence for the coexistence of other metabolic guilds of methanogens was obtained during a previous manipulation of sulfate concentrations. To fully characterize methanogenesis in these mats, in the absence of competition for reducing equivalents with sulfate-reducing microorganisms, we maintained microbial mats for longer than 1 year under conditions of lowered sulfate and salinity levels. The goal of this study was to assess whether observed differences in methane production during sulfate and salinity manipulation were accompanied by shifts in the composition of methanogen communities. Culture-independent techniques targeting methyl coenzyme M reductase genes ( mcrA) were used to assess the dynamics of methanogen assemblages. Clone libraries from mats sampled in situ or maintained at field-like conditions in the greenhouse were exclusively composed of sequences related to methylotrophic members of the Methanosarcinales. Increases in pore water methane concentrations under conditions of low sulfate correlated with an observed increase in the abundance of putatively hydrogenotrophic mcrA, related to Methanomicrobiales. Geochemical and molecular data provide evidence of a significant shift in the metabolic pathway of methanogenesis from a methylotroph-dominated system in high-sulfate environments to a mixed community of methylotrophic and hydrogenotrophic methanogens under low sulfate conditions. [ABSTRACT FROM AUTHOR]

Background: Apolipoprotein E ε4 (APOE4) allele is the strongest genetic risk factor for Alzheimer's disease (AD). Cognitively normal APOE4 carriers show an early decline in brain metabolic functions and gut microbiome dysbiosis before the onset of AD compared to APOE3 carriers. Our laboratory previously found that inulin, a prebiotic, is effective to restore metabolic functions and gut microbiome balance, and thus reduce risk for AD in an ApoE4 mouse model (Hoffman et al., 2019). However, whether the responses to the inulin diet are APOE allele‐dependent remains unknown. Therefore, our objective was to identify whether inulin would differently contribute to metabolic and gut microbiome changes due to APOE genotype. Method: We fed 3‐month‐old asymptomatic ApoE3 (E3FAD) and ApoE4 (E4FAD) mice a prebiotic inulin diet or a control diet containing cellulose for 4 months (N=15/group; Male:Female=1:1). After 4 months, we used magnetic resonance spectroscopy to measure in vivo brain scyllo‐inositol level, a compound that has been demonstrated to inhibit amyloid β aggregation (Fenili, Brown, Rappaport, & McLaurin, 2007). We collected the fecal samples for gut microbiome sequencing, and cecal and blood samples for metabolomic profiling. Result: Inulin induced scyllo‐inositol in hippocampus of the brain with a higher level in E4FAD mice. Inulin increased blood metabolites in tryptophan and tyrosine metabolic pathways that enhance nervous system in E3FAD mice. It increased blood metabolites in pentose phosphate pathway and citric acid cycle that support nucleotides and nucleic acids biosynthesis and energy production in E4FAD mice. These alterations in hippocampus and blood showed inulin's impacts on systemic metabolism depending on mouse ApoE genotypes. Inulin enhanced short chain fatty acids in cecum with a greater increase in E3FAD mice. E3FAD mice showed more distinct gut microbiome patterns between inulin and control groups compared to E4FAD mice. Conclusion: Inulin‐induced systemic metabolism and gut microbiome changes are APOE genotype‐dependent. Our study contributes to the gut‐brain axis research and potential AD prevention. Future studies can design human interventions that facilitate the guide of personalized nutrition in APOE3 and APOE4 population to prevent AD. [ABSTRACT FROM AUTHOR]